Analysis of nitric oxide synthase and nitrotyrosine expression in human pulmonary tuberculosis
Analysis of nitric oxide synthase and nitrotyrosine expression in human pulmonary tuberculosis
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DOI：
10.1164/rccm.2201023
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发表时间：
2002-07-15
影响因子：
24.7
通讯作者：
Chan, ED
中科院分区：
文献类型：
--
作者：
Choi, HS;Rai, PR;Chan, ED
一氧化氮（NO）在宿主防御人类结核病（TB）中的作用是有争议的。虽然实验证据表明，NO可能在控制结核病中发挥重要作用，但其在人类结核性肺中的表达尚未得到系统的表征。因此，我们研究了8例肺结核患者手术切除的肺组织中一氧化氮合酶（NOS）和硝基酪氨酸（后者是NO表达的标志物）的表达。免疫组织化学和形态学分析显示，与对照组相比，诱导型NOS，内皮型NOS和硝基酪氨酸，但不是神经元型NOS，显着升高的结核性肉芽肿的炎症区，并在非肉芽肿性肺炎区。肿瘤坏死因子-α（TNF-α）在结核性肺中也显著增加，主要局限于肉芽肿的坏死区域，在较小程度上局限于肉芽肿的炎症和纤维化区域。NOS亚型、硝基酪氨酸和TNF-α在肉芽肿内的上皮样巨噬细胞和巨细胞以及肺炎区域的肺泡巨噬细胞和上皮细胞中表达。这项描述性研究提供的证据表明，在人类结核病，NOS同工酶和NO存在于结核性肉芽肿的专门领域，其在人类结核病的确切作用仍有待确定。
The role of nitric oxide (NO) in the host-defense against human tuberculosis (TB) is controversial. Although experimental evidence indicates that NO may play an important role in controlling TB, its expression in human tuberculous lungs has not been systematically characterized. We therefore investigated the expression of NO synthases (NOS) and of nitrotyrosine, the latter a marker of NO expression, in surgically resected lungs of eight patients with TB. Immunohistochemical and morphometric analyses revealed that, compared with control subjects, inducible NOS, endothelial NOS, and nitrotyrosine, but not neuronal NOS, were significantly elevated in the inflammatory zone of the tuberculous granulomas, and in the nongranulomatous pneumonitis zone. Tumor necrosis factor-alpha (TNF-alpha) was also significantly increased in tuberculous lungs and was principally localized to the necrotic, and to a lesser extent, the inflammatory and fibrotic areas of the granulomas. The NOS isoforms, nitrotyrosine, and TNF-alpha were expressed by the epithelioid macrophages and giant cells within the granulomas and in alveolar macrophages and epithelial cells in pneumonitis areas. This descriptive study provides evidence that in human TB, NOS isoenzymes and NO are present in specialized areas of the tuberculous granulomas; their precise role in human TB remains to be determined.